Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure - Wikidata - awgldk - TriplyDB

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

http://www.wikidata.org/entity/Q35921523

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Cyclophilin D controls mitochondrial pore-dependent Ca(2+) exchange, metabolic flexibility, and propensity for heart failure in mice.Sildenafil and cardiomyocyte-specific cGMP signaling prevent cardiomyopathic changes associated with dystrophin deficiency An experimental approach to study the function of mitochondria in cardiomyopathy Cell death and survival through the endoplasmic reticulum-mitochondrial axis Mechanisms of altered Ca²⁺ handling in heart failure GLP-1 and cardioprotection: from bench to bedside Increased Echogenicity and Radiodense Foci on Echocardiogram and MicroCT in Murine Myocarditis Increased propensity for cell death in diabetic human heart is mediated by mitochondrial-dependent pathways DUSP6 (MKP3) null mice show enhanced ERK1/2 phosphorylation at baseline and increased myocyte proliferation in the heart affecting disease susceptibility Physical and functional interaction between calcineurin and the cardiac L-type Ca2+ channel Hexokinase II knockdown results in exaggerated cardiac hypertrophy via increased ROS production Mammalian target of rapamycin is essential for cardiomyocyte survival and heart development in mice The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability.Heart-specific deletion of CnB1 reveals multiple mechanisms whereby calcineurin regulates cardiac growth and function.Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.Dilated cardiomyopathy with increased SR Ca2+ loading preceded by a hypercontractile state and diastolic failure in the alpha(1C)TG mouse.Phospholamban ablation rescues sarcoplasmic reticulum Ca(2+) handling but exacerbates cardiac dysfunction in CaMKIIdelta(C) transgenic mice Temporal responses to intrinsically coupled calcium and zinc dyshomeostasis in cardiac myocytes and mitochondria during aldosteronism.Mitochondrial integrity: preservation through Akt/Pim-1 kinase signaling in the cardiomyocyte Pim-1 kinase protects mitochondrial integrity in cardiomyocytes.Electrophysiological remodeling in heart failure Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.Defective DNA replication impairs mitochondrial biogenesis in human failing hearts Calcineurin protects the heart in a murine model of dilated cardiomyopathy.Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy.Cellular and molecular pathways to myocardial necrosis and replacement fibrosis.{beta}1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways.Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.Mitochondrial pruning by Nix and BNip3: an essential function for cardiac-expressed death factors 20-HETE increases NADPH oxidase-derived ROS production and stimulates the L-type Ca2+ channel via a PKC-dependent mechanism in cardiomyocytes Two close, too close: sarcoplasmic reticulum-mitochondrial crosstalk and cardiomyocyte fate β-Adrenergic receptor stimulation causes cardiac hypertrophy via a Gβγ/Erk-dependent pathway.Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine Cardiac muscle regeneration: lessons from development.T-type Ca²+ signalling regulates aldosterone-induced CREB activation and cell death through PP2A activation in neonatal cardiomyocytes Role of the mitochondrion in programmed necrosis Dietary supplementation with docosahexaenoic acid, but not eicosapentaenoic acid, dramatically alters cardiac mitochondrial phospholipid fatty acid composition and prevents permeability transition.Functional and pharmacological characteristics of permeability transition in isolated human heart mitochondria.Mitochondrial hyperfusion during oxidative stress is coupled to a dysregulation in calcium handling within a C2C12 cell model.

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P2860

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

http://www.wikidata.org/entity/Q35921523

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2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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Journal of Clinical Investigation

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Ca2+- and mitochondrial-depend ...... mary mediator of heart failure

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P2093

Balvin H L Chua

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Christopher P Baines

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Hiroyuki Nakayama

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Hongyu Zhang

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Jeffrey Robbins

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Naser Jaleel

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Raisa Klevitsky

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Steven R Houser

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Timothy E Hewett

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Xiaoying Zhang

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P2860

PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts

Transgenic CaMKIIdeltaC overexpression uniquely alters cardiac myocyte Ca2+ handling: reduced SR Ca2+ load and activated SR Ca2+ release

The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure

FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death

Cell death: critical control points

Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Cellular basis of triggered arrhythmias in heart failure

Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1

Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemia

P304

2431-2444

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10.1172/JCI31060

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9

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117

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Jeffery D. Molkentin

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2007-09-01T00:00:00Z

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6145734

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1937500

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